p57 Kip2 Antibody [E16C13] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:100-1:1000 IP1:200-1:400 IHC1:50-1:500 IF1:50-1:500

Application
WB, IP, IHC, IF, ELISA

Reactivity
Human, Mouse, Rat

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
57 kDa

Positive Control	Mouse brain tissue; NIH/3T3 cells; Jurkat cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
p57 Kip2 Antibody [E16C13] detects endogenous levels of total p57 Kip2 protein.

Clone
E16C13

Synonym(s)
Cyclin-dependent kinase inhibitor 1C; Cyclin-dependent kinase inhibitor p57; p57Kip2; CDKN1C; KIP2

Background
p57Kip2, also known as cyclin-dependent kinase inhibitor 1C or CDKN1C, is a member of the Cip/Kip family of CDK inhibitors and acts as a potent tumor suppressor with restricted expression in specific tissues, being highest in the placenta, skeletal muscle, and heart. p57Kip2 is crucial for development and differentiation. It possesses a conserved N-terminal cyclin/CDK inhibitory domain that includes a cyclin-binding region, a CDK-binding site, and a 3₁₀ helix that blocks ATP hydrolysis in CDK2, as well as a unique central proline-alanine tandem repeat acidic domain and a C-terminal QT domain with a PCNA-binding motif. Phosphorylation at threonine 310 by cyclin E/CDK2 leads to recognition by the SCF-Skp2 E3 ligase, triggering ubiquitination and targeting p57Kip2 for proteasomal degradation. p57Kip2 binds and inhibits several G1/S phase cyclin-CDK complexes, especially cyclin E-CDK2, cyclin D2-CDK4/6, and cyclin A-CDK2 more effectively than cyclin B-CDC2, thereby enforcing G1 arrest and regulating the restriction point in the cell cycle. It can also facilitate the assembly of cyclin D1-CDK4/6 complexes. In addition, p57Kip2 sequesters LIMK-1, a Rho GTPase effector, to disrupt nuclear actin dynamics, inhibits JNK or SAPK pathways to regulate apoptosis and differentiation, and binds to PCNA to inhibit DNA replication. The N-terminal domain is essential for neurogenesis, gliogenesis, and cell cycle exit in cortical precursors, while the C-terminal regions independently govern neuronal migration. Knockout of p57Kip2 disrupts corticogenesis, myelination, and embryonic viability. Mutations in p57Kip2 are characteristic of Beckwith-Wiedemann syndrome, which is associated with cancer predisposition and various malignancies, while dysregulation through imprinting defects or Skp2 overexpression is implicated in tumorigenesis.

Background

p57Kip2, also known as cyclin-dependent kinase inhibitor 1C or CDKN1C, is a member of the Cip/Kip family of CDK inhibitors and acts as a potent tumor suppressor with restricted expression in specific tissues, being highest in the placenta, skeletal muscle, and heart. p57Kip2 is crucial for development and differentiation. It possesses a conserved N-terminal cyclin/CDK inhibitory domain that includes a cyclin-binding region, a CDK-binding site, and a 3₁₀ helix that blocks ATP hydrolysis in CDK2, as well as a unique central proline-alanine tandem repeat acidic domain and a C-terminal QT domain with a PCNA-binding motif. Phosphorylation at threonine 310 by cyclin E/CDK2 leads to recognition by the SCF-Skp2 E3 ligase, triggering ubiquitination and targeting p57Kip2 for proteasomal degradation. p57Kip2 binds and inhibits several G1/S phase cyclin-CDK complexes, especially cyclin E-CDK2, cyclin D2-CDK4/6, and cyclin A-CDK2 more effectively than cyclin B-CDC2, thereby enforcing G1 arrest and regulating the restriction point in the cell cycle. It can also facilitate the assembly of cyclin D1-CDK4/6 complexes. In addition, p57Kip2 sequesters LIMK-1, a Rho GTPase effector, to disrupt nuclear actin dynamics, inhibits JNK or SAPK pathways to regulate apoptosis and differentiation, and binds to PCNA to inhibit DNA replication. The N-terminal domain is essential for neurogenesis, gliogenesis, and cell cycle exit in cortical precursors, while the C-terminal regions independently govern neuronal migration. Knockout of p57Kip2 disrupts corticogenesis, myelination, and embryonic viability. Mutations in p57Kip2 are characteristic of Beckwith-Wiedemann syndrome, which is associated with cancer predisposition and various malignancies, while dysregulation through imprinting defects or Skp2 overexpression is implicated in tumorigenesis.

References
https://pubmed.ncbi.nlm.nih.gov/7729684/ https://pubmed.ncbi.nlm.nih.gov/20428755/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%